Coronary arteries are the major site for human atherosclerosis .CAD is considered the ultimate determinant of cardio vascualr health of our global population.Coronary atherosclerosis has a predilection for proximal sites and branching points.Typically it occurs in leftmain, LAD ostium, LCX ostium, proximal LAD, diagonal origins, OMs RCA and its branches .
Septal branches , even though divide very early from the LAD , it is uncommon to get affected by coronary atherosclerosis. Even for an experienced interventional cardiologist , it would be very rare to have performed a PCI for septal disease.
Why septal branches of LAD is rare to suffer from atherosclerosis ?
We don’t know the answer yet.
But , it is thought,septal branches are near perpendicular branches .The branching angle and incidence of atherosclerosis has a peculiar relationship.IAt any bifurcation point , the atherosclerosis tend to occur , if the angle is more acute , and is less common in abtuse angles .It is almost rare , if branching happens at exact 90 degree angle or so !
The other reason for septal branches being immune to atherosclerosis is , it runs within the muscle in its major course. The constant squeezing action(. . . and possibly bridging also) makes it difficult for the process of atherosclerosis to sustain and grow .
Can you still get a septal CAD ?
Yes, usually as a component of bifurcation or trifurcation lesion. Some times a diagonal and septal are very close together and atherosclerosis involves both ostia.
What is the implication for the cardiologist to perform a PCI with stenting in a septal branch of LAD ?
PCI and stenting in the septal branches are more prone for crushing and fracture as it is constantly exposed to the mechanical effects of muscle contraction.
Any other significance for septal branches of LAD ?
Isolated septal myocardial infarction can occur.This could be even a embolic manifestation.
Septal branches of LAD are potential target for therapeutic embolisation (By injecting alcohol) in patients with hypertrophic obstructive cardiomyopathy(HOCM) .This manover aims to produce a controlled septal myocardial infarction and thus paralysing the left ventricular outflow tract and reduce the dynamic LVOT gradient. This form of treatment, was glorified till recently now considered experimental !
Contrary to popular belief ,great things happen only rarely in medicine . It takes only few months of training or workshops , for a wrong or inappropriate concept to percolate our brains ! But , it would require, decades of time , energy and efforts , for correcting that wrongly assimilated concept in medicine!
Interventional cardiologists are among the rare breed of physicians, who always believe in evidence ! But , the quality of the evidence is rarely questioned ! 30 years of PCI & 20 years of stenting has failed our common senses ! Fortunately , today, we have 135 pages of new evidence ( Not really new , old evidence interpreted with sound logic !)
Hats off to ACC and associates for bringing out this much belated appropriateness guidelines for the interventional cardiologists.
ACCF/SCAI/STS/AATS/AHA/ASNC 2009 Appropriateness Criteria for Coronary Revascularization
A Report of the American College of Cardiology Foundation Appropriateness
Criteria Task Force, Society for Cardiovascular Angiography and Interventions,
Society of Thoracic Surgeons, American Association for Thoracic Surgery,
American Heart Association, and the American Society of Nuclear Cardiology
Endorsed by the American Society of Echocardiography, the Heart Failure Society of America, and the
Drug eluting stents : A slap on the face of Evidence based cardiology . . .
Click the BMJ link or read below
It is often said science is sacred and unfortunately we forget , science is not a heavenly creation and it is the creation of scientist of varying grades of integrity fueled by the vested interest of medical industry . It has been a almost a daily affair , some of the devices and drugs are recalled or found to be unsafe on patients.
Now the big cat has come out .The Drug eluting stent has fallen from Hero to Zero in a short span of 5 years. It was projected to have zero percent restenosis in 2002 . And now we realize it is Zero percent truth.
What has started as anecdotal reports of late stent thrombosis has indeed become an epidemic in all DES patients. The five studies that has been published in the NEJM this month (March 2007) has convincingly proved how unsafe these stents are in most of the coronary population .
Millions of patients in whom this stent was implanted will carry an impending stent thrombosis and possibly an SCD . Who is to take care of them ?
The DES story is a clear cut case of getting premature approval for a dangerous form of treatment inside human coronary arteries.
It is amazing how the scientist’s eyes are shut by the illusion of knowledge and lure of wealth. How foolish they were to think drug which was administered via the stent will selectively prevent vascularisation and leave the normal endothelium intact . Now they realized , one should not suppress the endothelial growth around the stent and got the fundamental point wrong. Which was the key reason for the astonishing episodes of late stent thrombosis. When we play with biology of nature we have to be little more careful .God has created man and his heart for over a million years . One can not alter it by a 6 month follow up study of DES .
When ICDs were exposed last year , of similar disastrous outcome they were recalled and explanted . How are we going to unstent the millions of coronary arteries ?
Somewhere along the line the medical professionals have lost the battle against the Wall street and NASDAQ . Or how else we can explain repetition of similar events.
The wages for the modern technology , the patients have to pay a heavy price.
Let us all hope common man with common sense will reign supreme over the sixth sense of the uncommon man . . .
“Ignorance is better than illusion of knowledge”
Dr Venkatesan Sangareddi MD , Assistant Professor of cardiology , Madras medical college Chennai, India
Anginal pain is a type of visceral pain.It is carried by type C unmylinated nerve fibres.The perception of angina is a complex process.It is a combination of visceral and cutaneous referral pain.
How often is angina silent in diabetes mellitus ?
Presence of diabetes per se does not make an angina silent. In fact, if one takes 100 patients with diabetes , if angina occur in them , it is more often , manifest than silent. So , only few of the diabetic patients who develop diabetic autonomic neuropathy fail to have angina.The exact incidence is not known.It could be around 20%.
If angina can be silent in diabteics , can they have anginal equivalents ?
This again is not answered in literature. Among the anginal equivalents , the most common is dyspnea , which can occur in diabetics.But now , we know dyspnea also needs thoracic nerve signals from the intercostal muscle spindle and colgi organs.This can also be impaired in diabetics.
Can silent and mainfest episodes occur in a same patient ?
Yes.
Once silent does not mean always silent, and similarly once angina is felt it does not mean he is going to feel the next episode as well !
This strongly reminds us medical science is much a complex subject and what we know is very little in pain perception.
How is silent ischmia different from silent angina ?
There is considerable overlap between silent ischemia and silent angina
The questions to be answered are
Which is silent ? Is it the angina or is it the ischemia or both ?
Silent ischemia can occur in any individual , this is also called as silent CAD . When ischemia occurs but fails to generate pain it is silent ischemia .Undiagnosed CAD in asymptomatic individuals is also called silent ischemia or CAD.In this population Exercise stress testing detects CAD which was otherwise silent and masked.These patients may develop angina during EST.
During exercise stress testing many times patient has significant ST depression more than 2mm but still chest pain may not occur.These episodes may either be silent ischemia or ngina. Many times the EST is terminated before angina is manifest .( Chest pain is the last to occur in the chain of events following ischemia- Concept of ischemic cascade )
What are the other situations where angina can be silent ?
Pain perception and threshold level is high , so patient indeed has anginal signals but fails to feel it .
Patients on antianginal medication , fail to feel the angina.
Chronic betablocker therapy can exactly mimic autonomic neuropathy
Is it a blessing for the patient to have painless episodes of angina ?
When their ischemic colleagues , suffer a lot with chest pain it is tempting to think these diabetic patients are blessed!
Scientifically , this could be true in at least in some especially in a patients who’s coronary anatomy is known and devoid of any critical proximal lesions. For example a small PDA lesion can produce severe angina , but may be silent in diabetic and be comfortable .This lesion is insignificant other wise * !
It should also be recalled , pain relief has been an important goal for treatment of CAD .In olden days, thoracic sympathectomy was done for angina . In fact , even in CABG , one of the the mechanisms for angina relief is attributed to cardiac denervation.
Caution: Even a small episode of ischemia can trigger an electrical event .But it is rare.
How common is silent infarct (STEMI) in diabetic patients ?
In a simple questionnaire we asked the diabetic patients in our CCU how they felt their pain during MI.Most felt it normally as do other non diabetic . Diabetes does not make all anginal episodes silent. Severe episodes of ischemia may be painful while less severe episodes may be painless. Diabetic autonomic neuropathy is a least recognized and poorly understood complication of diabetes.Diabetes , involves the vasanervorum of the autonomic nerves.
The other mechanisms postulated in diabetic neuropathy are
Reduction in neurotrophic growth factors.
deficiency of essential fatty acids .
Reduced endoneurial blood flow and
Nerve hypoxia .
Is diabetic autonomic neuropathy treatable ?
Very difficult problem indeed.Controlling diabetes may partially correct the neural dysfunction.Many add on neuro vitamins and aminoacids are having a good market !
If you successfully treat diabetic autonomic neuropathy will my patient start feeling the hitherto silent episodes of angina ?
We don’t know.Logic would answer ” YES”
What is the ultimate effect of cardiac autonomic neuropathy.
The growth of medical science has been phenomenal .It is estimated , the quantum of break throughs and development in the last 50 years is nearly equal to 2000 years of evolution of our knowledge put together. Along with this growth , came the unavoidable misuse , and abuse of medical science. This is mainly due to contamination of medicine with commerce . Federal drug authority (FDA) and it’s variants were formed in all countries to monitor the proper usage of these technologies for the benefit of mankind. It has an authority to ban a drug or device , if it is found to bring more injury or side effects than benefit !
But , unfortunately there is no legal authority to ban an an investigation which is potentially or (really harmful )
or used extensively without any valid purpose .
The list of such investigation is increasing in every speciality
In cardiology
Doing a Troponin assay in patients wuth classical STEMI
MDCT in general population
Pro BNP in all suspected cardiac failure
Routine C reactive protein for CAD
Central venous catheters for all pateints with shock.
Is there a case for banning an investigation (Like banning a drug) for the benefit of our patients ?
Looking superficially , it may seem ironical. But we realise many seemingly innocuous investigations are responsible for uncontrolled misery for many patients.
This especially true in people who throng the wellness clinic (Also called master health check up)
A incidentally high C – reactive protein can lead on to forearm blood flow assessment of endothelial dysfunction and carotid intimal plaque that could lead onto carotid stents ! and life long anticoagulation , and an excess INR and sudden cerebral bleed and death !
This is one sample story in one particular speciality
There is a definite case for banning ( Either total or partial) some of the questionable investigations which are done routinely !
Just because these investigation do not have any physical , visible , adverse reactions like a drug , it should not be allowed to be abused .The consequence of false positive results of these investigations could be terrible and worse than the real disese itself !
Ventriculophasic sinus arrhythmia is a non-respiratory sinus arrhythmia seen in complete AV block.
The PP interval enclosing a QRS complex is shorter than a PP interval not enclosing a QRS.
The Mechanism
The proposed mechanism is the increased blood flow into the SA node artery during ventricular systole stimulating it to produce an early pacemaker activity and thus shortening the sinus cycle length.
Clinical significance : None for the patient Academic purpose for the students
Coronary arterial circulation is the life line for the human heart and it’s survival.Typically it is supplied by two coronary arteries, left and right coronary artery.Both, together carry about 250ml of blood every minute.( Approxinately equal to a cup of coke ! ).These coronary arteries generally divide in a predetermined fashion , and have multiple branches . It is a mystery , what decides this branching pattern
Is it like a our palmar crease ? or the cerebral gyri ?
However , it does follow a certain rule, one major coronary artery will follow the four important grooves of heart. In the left side , left main coronary artery (LM) originates in the left coronary sinus (Size varying between 1mm -20mm) and usually bifurcates into LAD and LCX. The left anterior descending artery (LAD) runs in anterior interventricular groove while , the right atrio ventriculo groove carries the right coronary artery(RCA) .Left circumflex artery (LCX) traverses the left atrio ventricular groove.The most inconstant branch is the posterior descending artery (PDA) which runs in the posterior interventricular groove.PDA can arise from either RCA, LCX or both or even from LAD.
The major branches of LAD are called diagonal and septal while the branches of LCX are called obtuse marginal(OM).There can be two to three diagonal and OMs.
What is ramus intermedius coronary artery ? What is the incidence of Ramus ?
The left main coronary artery instead of bifurcating into two , it trifurcates into three vessels.(LAD, LCX, Ramus)
The real incidence could vary betweenn (10% to 30%) depending upon the series.
What course it takes ?
It generally goes in the angle between the LAD and the LCX.It may either behave like a large OM or a diagonal branch.It supplies the lateral free wall of the LV many times.The peculiarity of this vessel is it does not run in a anatomical groove .It simply slides over the free surface of LV.Rarely, a very abnormal course of ramus, criss cross the aorta and pulmonary artery .
How common is atherosclerosis within Ramus ?
We don’t know yet. But it is very likely since it is an early branch from left main, it might have a predilection for atherosclerosis as like LAD or LCX ostium.In fact now we recognise more of trifurcation lesions involving three branches of left main .
What would be the ECG finding if a large ramus is the culpirit vessel during STEMI ?
This scenario could be rare.
ACS in ramus could present as ST elevation in 1/Avl /V5,V6
Lateral MI
Apical MI
High lateral MI
But it is realised , whenever the ECG changes are not fitting with typical ASMI or a lateral MI one should suspect a ramus lesion
What is the significance of ramus for an interventional cardiologist ?
PCI in ramus is a rare opportunity for a cardiologist .The issue here is, if ramus is involved adjacent LAD and LCX is also likely to be involved .So it would logically be a multivessel , complex angioplasty.Isolated ramus lesion could be tackled easily.Another issue here could be ,since this vessel is not within any anatomical groove stent deployment would have a poor support and prone for mobilisation and migration .
Stents are mechanical devices like a spring , used to keep an artery open after a PTCA or PCI.
Bare metal stents(BMS) were found to have restenois rate of about 25%. So it was perceived a stent should have it’s own protective coat , so that it won’t get restenosed.For this the researchers thought anti cancer drugs are ideal as they block cell proliferation and thus neovascualrisation and restenosis.Alas, they were found dismally wrong , after all , neointiaml proliferation is only a part of the problem of restenosis and simple blocking of cell growth is insufficient . The issue doesn’t stop with that, the anti cancer drugs incorporated within the stent simply can not differentiate normal from abnormal cells and
DES effectively blocks the normal endothelisation over the stents and make this highly vulnerable for acute stent thrombosis .
This complication is unique to DES and can result in SCD.Further ,during the last 6 years of DES , we recognised the restenosis rate has increased form the much hyped O % to almost 15% and it’s still growing . These complications has made a huge question mark over the future of drug eluting stents !
The concept of DES may not die , but which drug it should elute should be answered ! This again is going to be a long battle. So it is currently adviced, based on common sense ( With due respects to those RCTs funded by industry )
Whenever you encounter a block within the coronary artery* Ask the following questions in sequence ,
Whether we can leave it alone with medical therapy , if the answer is no , proceed to the next step !
Is there a possibility for plain balloon angioplasty in a given vessel (POBA, Yes ! the concept is not dead yet !)
If you decide a stent is required , Will the bare metal do the job ?
In multivessel CAD , Did the issue of increased metal load on the long term outcome was considered ?
If lesions appear complex, should we notstrongly consider CABG as an option ?
However if we have the habit of ask ing the following question you are likely to deviate from scientific approach
Is it possible to put a stent across the block ?
Yes , will be the answer most of the time ,and the patient will invariably get one or more stents and carry a life long stent related problems.
*The rule does not apply in Acute coronary syndromes
Also read this letter posted by the author published in British medical journal
One of the important principles of post PCI care is, we need to be very careful till the metal struts are fully endothelialised . This is of vital importance as improper endothelialisation is a powerful trigger and nidus for a imminent thrombosis and acute coronary syndrome.
It is a billion dollor irony , the much hyped DES does exactly what we don’t want ! and still it’s usage is increasing world wide . The drugs (Anti cancer agents) which coat the DES are the villains as it prevents the metal struts from being endothelialised and keep the metal surface raw and vulnerable , while the much maligned bare metal stents allow this natural endothelialisation process without any interruption ! So right now it is mandatory to administer dual antiplatelet agents life long( life of the stent !) for the patients with DES.
Just look , at the following image of a stent in vitro at 30 days follow up
HT management has been made easier with the availability of many good drugs , at the same time it has become a complex issue with as many classification and guidelines.
The management of HT has evolved over the decades. Now we have realised HT is not a simple number game. Reducing the blood pressure to target levels is not sufficient and is not the primary aim !.
In fact we now know controlling the numbers alone is never going to work , combined risk factor reduction is of paramount importance.
HT per se is less lethal but when it combines with hyperlipidemia and diabetes or smoking it becomes aggressive.The blood lipids especially the LDL molecule enjoy the high pressure environment , penetrate and invade the vascular endothelium.
ASCOT LLA study has taught us, for blood pressure reduction to be effective and reduce CAD events one has to reduce thier lipid levels also.So , for every patient with HT there is not only a target BP but also a target LDL level .
Final message
The tip for better vascular health is, all hypertensive patients should keep their lipids to optimal levels and all hyperlipidemia patients should keep their BP as low as possible .
“Keep your LDL as low as your diastolic blood pressure and let us keep it around 70 -80
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